The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Nitric Oxide Suppression of Apoptosis Occurs in Association with an Inhibition of Bcl-2 Cleavage and Cytochrome cRelease
Open accessAbstract
It is now known that caspase-3-like protease activation can promote Bcl-2 cleavage and mitochondrial cytochrome c release and that these events can lead to further downstream caspase activation. NO has been proposed as a potent, endogenous inhibitor of caspase-3-like protease activity. Experiments were carried out to determine whether NO could interrupt Bcl-2 cleavage or cytochrome c release by the inhibition of caspase activity linking these events. NO inhibited the capacity of purified caspase-3 to cleave recombinant Bcl-2. Both Bcl-2 cleavage and cytochrome c release were inhibited in tumor necrosis factor alpha- and actinomycin D-treated MCF-7 cells exposed to NO donors. The NO-mediated inhibition of Bcl-2 cleavage and cytochrome c release occurred in association with an inhibition of apoptosis and caspase-3-like activation. Thus, NO suppresses a key step in the positive feedback amplification of apoptotic signaling by preventing Bcl-2 cleavage and cytochrome c release.
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“NO is a well-characterized regulator of mitochondrial function that inhibits cytochrome c oxidase, decreases mitochondrial ROS formation, and limits apoptotic cytochrome c release [32–36].”
From Inorganic nitrite therapy: historical perspective and future directions (2011) · cites this paper as [36]
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Yalcin, A., Soddu, E., Turunc Bayrakdar, E., Uyanikgil, Y., Kanit, L., Armagan, G., Rassu, G., Gavini, E., & Giunchedi, P. (2016) · Journal of Pharmaceutical Sciences · doi:10.1016/j.xphs.2016.05.017 · Cited by 37
Effects of long term nitrite therapy on functional recovery in experimental ischemia model
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Metadata
- Authors
- Kim, Y.-M., Kim, T.-H., Seol, D.-W., Talanian, R. V., & Billiar, T. R.
- Affiliations
- Kangwon National University (KR)
- University of Pittsburgh (US)
- Corresponding author
- Billiar, Timothy R.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 1998-11
- Volume
- 273
- Issue
- 47
- Pages
- 31437-31441
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2077925191
- Cited by
- 245
- References
- 36
- Citations by year
- 2024: 3 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 1 · 2019: 3 · 2017: 5 · 2016: 2 · 2015: 3 · 2014: 1 · 2013: 7 · 2012: 7
- FWCI
- 8.04
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institute of General Medical Sciences (R01GM044100, R01 GM 44100)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- nitric oxide, apoptosis, cytochrome c release, caspase-3, caspase inhibition, mitochondrial apoptosis, MCF-7 cells, TNF-α, actinomycin D
- MeSH terms
- Cytochrome c Group, Dactinomycin, Enzyme Activation, Liver, Nitric Oxide, Penicillamine, Tumor Necrosis Factor-alpha, Signal Transduction, Apoptosis, Proto-Oncogene Proteins c-bcl-2, Caspase 3, Caspase Inhibitors
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